sepsis guidelins and stop sepsis

8/10/2019 Sepsis Guidelins and STOP SEPSIS

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Sepsis Guidelines,and The

STOPSepsis(Strategies to Timely Obviate

the Progression of Sepsis )

Basrul Hanafi

Division Of Digestive SurgeryHasan Sadikin General Hospital


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Sepsis Guidelines

I. Background

Mortality rate of peritonitis with concomitantseptic shock, more than 60%

If More than 4 MOFS already occured,

mortality rate nearly 100 % (Baue,2000).

Early Tratment of MODS and Preventing the

MOFS, mortality rate are able to reduce

(1995., Boyd, 1993., Flemming, 1992., Yu, 1993).


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Sepsis:

A Major Cause of ICU Death

More than 750,000 cases of severe sepsis in the

US each year

Mortality about 20% (recent decline)Economic cost of $17 billion each year

Incidence is projected to increase by 1.5% yearly

Although prognosis has improved, because ofincreased incidence, actual deaths will increase


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SIRS

Pancreatitis

BurnsTrauma

Others

Bacteremia

Fungemia

Parasitemia

viremia

Infection

Sepsis

Relation between infection, sepsis, SIRS and MOF

The systemic

inflammatory

response syndrome

(SIRS) produces aclinical reaction that

is indistinguishable

from sepsis in the

absence of an

infecting organism

Timothy W Evans, Mark Smithies: Organ dysfunction,

Clinical review. BMJ VOLUME 318 12 JUNE 1999

Local

inflamation

Distantinjury

Multi-Organ

failure


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The Sepsis Continuum

A clinical responsearising from anonspecific insult, with2 of the following:

T >38oC or 90 beats/minRR >20/minWBC >12,000/mm3or

10% bands

SIRS = systemic inflammatoryresponse syndrome

SIRS with a

presumed

or confirmed

infectiousprocess

Chest 1992;101:1644.

SepsisSIRSSevere

Sepsis

Septic

Shock

Sepsis with

organs failure

Refractory

hypotension

Lactat 2-4, >4mmol/L

Low, HightRisk


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Comparison With

Other Major Diseases

National Center for Health Statistics, 2001.American Cancer Society, 2001. *American Heart Association.2000.Angus DC et al. Crit Care Med.2001;29(7):1303-1310.

AIDS* Colon Breast

CancerCHF Severe

Sepsis

Cases/100,0

00

0

50

100

150

200

250

300

Incidence of Severe Sepsis Mortality of Severe Sepsis

0

50,000

100,000

150,000

200,000

250,000

Deaths/Year

AIDS* Severe

SepsisAMIBreast

Cancer


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Grading of Recommendations

Supported by at least two level I investigations

Supported by one level I investigation

Supported by level II investigations only

Supported by at least one level III investigation

Support by level IV or V evidence

Guidelines :

Based Medicine(EBM)Grading System


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I. Large randomized trials with clear-cut results; low risk offalse-positive (alpha) error or false-negative (beta) error

II. Small randomized trials with uncertain results; moderate-to-high risk of false-positive (alpha) and/or false-negative (beta)error

III. Nonrandomized, contemporaneous controlsIV. Nonrandomized, historical controls and expert opinion

V. Case series, uncontrolled studies, and expert opinion

Grading of Evidence

Grading System


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1. Initial Resuscitation

2. Diagnosis

3. Antibiotic Therapy

4. Source Control5. Fluid Therapy

6. Vasopressores

7. Inotrophic Therapy

8. Steroid

9. Recombinant HumanActivated Protein C(rhAPC) [drotrecoginalfa (activated)]

10.Blood Product Administration

11.Mechanical Ventilation

12.Sedation, Analgesia, and Neuromuscular

Blockade in Sepsis

13.Glucose Control

14.Renal Replacement

15.Bicarbonat Therapy

16.Deep Vein Thrombosis Prophylaxis

17.Stress Ulcer Prophylaxis

18.Limitation of Support

Establish EBM on Sepsis


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Summary of SSC Guidelines

Initiative GradeDVT prophylaxis with low dose heparins or

mechanical devicesA

Stress ulcer prophylaxis, preferably with H2blockers ADo not use more then 300 mg/day hydrocortisone A

Weaning protocol with spontaneous breathing trials A

Do not increase cardiac index to supranormal

AEarly initial resuscitation to goals B

Red blood cell transfusion/dobutamine to goals B


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Summary of SSC Guidelines

Initiative GradeDo not use low dose dopamine for renal protection B

rh Activated Protein C [drotrecogin alfa(activated)] in patients with high risk of death

B

RBC transfusion if hemoglobin


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Target Resusitasi pada

Tingkat Seluler


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Cellular metabolism in the shock state

Respiratory

Enzyme

Chain

Citric

Acid

Cycle

GlycolysisGlucose Pyruvate

Lactate

NAD+

NADH

ANAEROBIC

AEROBIC

CO2

Oxygen

2ATP

36ATP

H2O

NAD+

NADH


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Aerobic Metabolisms


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Anaerobic Metabolisms


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Target Pada Tingkat

Mikrosirkulasi


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Microcirculatory System


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Rheology of Erythrocyt


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Shock state

DIVERTED BLOOD FLOW

HEART & BRAIN

Control ofCV system

Spinchterclosed

Vasoconstriction

NORMAL


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DISTAL ILEUM SECTION


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Target on Macrosirculation :Hemodynamic, Oxygen Transport

Parameters


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DO2 and VO2 on Severe Shock

Riverss Concepts (2002) Balanced DO and VO through


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Riverss Concepts(2002) Balanced DO2and VO2through

Balancing Cardiac Preload, Contractility, and Afterload

Cardiac preload

(EDI)

Cardiac after load

(SVR)

Cardiac contractility

(CI)

Balance between DO2 and VO2

SvO2 Lactate Base deficit pH

Resuscitation end points

Target forhemodynamic

Surrogate forcardiac index

V l f S O2


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Value of SvO2

SvO2

Low SvO2

SvO2 < 50%

Poor tolerated

Below 30%

Anaerobic Metabolism

Lactic Acidosis

Emergency

High SvO2

Have enough O2 available

to the cells but the cells

cannot extract it

Shunt, intracardiac or

systemic vascular

shuntHb failed to unload O2

(leftward shift in ODC)

Interstitial edema

Toxic, Dying or Necrotic

Tissue hypoxia

Acute DO


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O2ER = 25%

Acute DO2

VO2O2ER = 50%

O2return

500SvO2 50%

Anemia

CO

Hypoxemia


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Pencegahan & Pengelolaan


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Initial

physiologiccondition

I st Initial StagesOf PhysiologicDerangement

CNSCardiovascular

HormonalMetabolic

Immune system

and mediators

NewEquilibrium:II nd or rd etc

(New Stages of

physiologicDerangement)

Death ?Sequels?

Phi losophy of Phys io log ic

Derangement

2ndHIT

Goals

DirectedResuscitation

Supportive Th/1stHIT

Insult/Injury


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Introduction

The Management of Sepsis and Trauma

Source Control

Nutrition / MetabolicSupport

Resuscitation &

Physiologic Support1. Minimize flow-dependent

oxygen consumption

2. Minimize flow-dependent

lactate clearance

3. Restore Microcirculation

1. Remove / Treat Infection2. Remove / Treat Inflammation

3. Remove Dead Tissue

4. Stabilization Injured Tissue


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P i P it iti U


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Prognosis Peritonitis Umum e.c

Perforasi Ileum demam tifoid

(Hanafi, 1979)

Keadaan Umum Pre Op (Setelah Resusitasi)

i. KU baik, Mortality < 5 %

ii. KU sedang Mortality 25 %

iii. KU tetap buruk pasca Resusitasi, Mortalitymendekati 100 %

Upayakan KU Baik, EGDT Pola Kita Sejak1979


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Numerik Asli TKF vs TKU

Analisis Multivariet Numerik AsliTingkat Kekacauan Fisiologik (Gabungan)

Antar Kelompok RTNI vs RTSK

=.00729

CIEDISSVRILactateCCr

Kelompok RTNI

Resus

Jam 00

Jam 12

Jam 24

Jam 48-50

0

50

100

150

200

250

300

Kelompok RTSK

Resus

Jam 00

Jam 12

Jam 24

Jam 48

Analisis Multivariet Numerik AsliTingkat Keadaan Umum (Gabungan)

Antar Kelompok RTNI vs RTSK

p=.91224

HRMAPS st BP

Kelompok RTNI

Resus

Jam ke 00

ke 12

ke 24

ke 4870

80

90

100

110

120

130

140

150

Kelompok RTSK

Resus

Jam ke 00

ke 12

ke 24

ke 48


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Numerik Asli RTNI vs RTSKKelompok Heart Rate MAP Syst BP

Jam ke 0 12 24 48 0 12 24 48 0 12 24 48

RTNI 106 95 94 87 87 83 82 87 116 111 113 121

RTSK 106 100 94 103 92 91 90 97 125 124 123 131

Kelompok CI EDI SSVRI

Jam ke 00 12 24 48 00 12 24 48 00 12 24 48

RTNI 3.9 4.0 3.8 3.9 63.0 68.9 67.9 73.4 200.3 159.8 174.7 151.0

RTSK 3.9 4.7 3.6 3.1 64.3 71.3 63.8 56.4 198.6 172.6 183.9 230.5

Kelompok Lactate CCr

Jam ke 00 12 24 48 00 12 24 48

RTNI 1.7 1.6 1.4 1.3 43.1 60.0 83.3 98.0

RTSK 1.9 1.5 1.4 1.3 72.0 58.9 55.1 52.7


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KU Konvensional vs TKF

KU Konvensional RTNI vs RTSKp=.91224

Kelompok RTNIKelompok RTSK

1 2 3 4

Resusitasi

0.5

1.0

1.5

2.0

2.5

3.0

3.5

4.0

4.5

KU

KF Antar Kelompok RTNI vs RTSKp=.13144

Kelompok RTNIKelompok RTSK

Jam ke 00

Jam ke 12

Jam ke 24

Jam ke 48

Resusitasi

0.8

1.0

1.2

1.4

1.6

1.8

2.0

2.2

2.4

KF


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Kelompok RTNI lebih baik dari RTSK dalam

memperbaiki KF (Kekacauan Fisiologik)

Analisis Multivariet KF Antar Kelompok RTNI vs RTSK

p=.04604

CI

EDI

SSVRI

Lactate

CCr

Kelompok RTNI

ResusJam ke 00

Jam ke 12Jam ke 24

Jam ke 48-0.5

0.0

0.5

1.0

1.5

2.0

2.5

3.0

3.5

4.0

4.5

Kelompok RTSK

ResusJam ke 00

Jam ke 12Jam ke 24

Jam ke 48


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RTNI lebih baik daripada RTSK dalam

memperbaiki Hemodinamik Sistemik, Fungsi

Ginjal, Status Metabolik

Analisis Waktu ke waktu Kekacauan Fisiologik

Antar Kelompok (WW*Kel.RTNI vs RTSK)

Wilks lambda=.38699, F(15, 21)=2.2176, p


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- Central Venous Pressure 8-12 mm Hg (12-15 in ventilator pts)

- Mean arterial pressure > 65 mm Hg

- Urine output > 0.5 mL/kg/hr

- ScvO2or SvO2 70%;

if not achieved with fluid resuscitation during first 6 hours:

- Transfuse PRBC to hematocrit > 30% and/or

- Administer dobutamine (max 20 mcg/kg/min) to goal

Resuscitation should begin as soon as severe sepsis or sepsis

induced tissue hypoperfusion is recognized

Elevated Serum lactate identifies tissue hypoperfusion in

patients at risk who are not hypotensive

Goals of therapy within first 6 hours are Grade B

Initial Resuscitation

-

Protocol for Early Goal-Directed Therapy (EGDT)


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Protocol for Early Goal-Directed Therapy (EGDT)

Supplement O2Endotracheal intubations

Mechanical ventilation

Central venous andarterial catheterization

Sedation, Paralysis(if intubated), or both

CVP

MAP

ScvO2

Crystalloid

Colloid

< 8 mmHg

Vasoactive agents< 65 mmHg

> 90 mmHg

812 mmHg

6590 mmHg

70%

Goalachieved

Transfusion of RCuntil Ht 30%

70%

< 70%

Inotropic agents

Hospital admissionYesNo

< 70%

Study design


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Study designSIRS criteria

SBP < 90 mmHgLactate > 4 mmol/L

Assessment and consent

Randomization (n=263)Standard Therapy

in ED (n=130)Early goal-directedtherapy (n=133)

Vital sign, Lab data, cardiacmonitoring, pulse oximetry,

Urinary catheterization,

arterial and venouscatheterization

Continuous SvO2monitoring and

EGDT for 6 hours

CVP 8-12 mmHg

MAP 65 mmHg

Urine 0.5 cc/kg/min

ScvO2 70%

SaO2 93%

Hematocrit 30%

Cardiac index

VO2

CVP 8-12 mmHg

MAP 65 mmHg

Urine 0.5cc/kg/min

Standard care

Hospital admission

Vital sign, lab data,obtained every 12 hour

for 72 hour

Follow upDid not complete6 hour (n=13)

Did not complete6 hour (n=14)

Early Goal Directed Therapy


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49.2%

33.3%

0

10

20

30

40

50

60

Standard Therapyn=133

EGDTn=130

P = 0.01*

*Key difference was in sudden CV collapse, not MODS

28-day Mortality

Early Goal-Directed Therapy

Results


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ALGORITM

Mortality 60% 20-40% 10-20% 0-10%


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CLINICAL PATHWAY


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Admission Day I


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Day II - VII


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sepsis guidelins and stop sepsis

Documents

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